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Fenfluramine: Wikis


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Systematic (IUPAC) name
CAS number 458-24-2
ATC code A08AA02
PubChem 3337
DrugBank 3337
ChemSpider 3220
Chemical data
Formula C12H16F3N 
Mol. mass 231.26 g/mol
Pharmacokinetic data
Half life 20 hours
Therapeutic considerations
Pregnancy cat.  ?
Legal status Uncontrolled
Routes Oral
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Fenfluramine is a drug that was part of the Fen-Phen anti-obesity medication (the other drug being phentermine). Also known as Pondimin, Ponderax and Adifax; fenfluramine was introduced on the U.S. market in 1973. It is the racemic mixture of two enantiomers, dextrofenfluramine and levofenfluramine. It increases the level of the neurotransmitter serotonin, a chemical that regulates mood, appetite and other functions. Fenfluramine causes the release of serotonin by disrupting vesicular storage of the neurotransmitter, and reversing serotonin transporter function.[1] The end result is a feeling of fullness and loss of appetite.


Withdrawal due to heart disease

The drug was withdrawn from the U.S. market in 1997 after reports of heart valve disease,[2][3] and pulmonary hypertension, including a condition known as cardiac fibrosis. After the US withdrawal of fenfluramine, it was also withdrawn from other markets around the world.

The distinctive valvular abnormality seen with fenfluramine is a thickening of the leaflet and chordae tendineae. One mechanisms used to explain this phenomenon involves heart valve serotonin receptors, which are thought to help regulate growth. Since fenfluramine and its active metabolite norfenfluramine stimulate serotonin receptors 5-hydroxytryptamine (5-HT) this may have led to the valvular abnormalities found in patients using fenfluramine. In particular norfenfluramine is a potent agonist of 5-HT2B receptors, which are plentiful in human cardiac valves. The suggested mechanism by which fenfluramine causes damage is through over or inappropriate stimulation of these receptors leading to inappropriate valve cell division. Supporting this idea, is the fact that this valve abnormality has also occurred in patients using other drugs that act on 5-HT2B receptors.[4].

According to a study of 5743 former users, damage to the heart valve continued long after stopping the medication [5]. Of the users tested, 20 percent of women, and 12 percent of men were affected. For all ex-users, there was a sevenfold increase of chances of needing surgery for faulty heart valves caused by the drug.


  1. ^ Nestler, Eric J. "Molecular Neuropharmacology: A Foundation for Clinical Neuroscience" McGraw-Hill, 2001.
  2. ^ Connolly HM, Crary JL, McGoon MD, et al (1997). "Valvular heart disease associated with fenfluramine-phentermine". N. Engl. J. Med. 337 (9): 581–8. doi:10.1056/NEJM199708283370901. PMID 9271479. 
  3. ^ Weissman NJ (2001). "Appetite suppressants and valvular heart disease". Am. J. Med. Sci. 321 (4): 285–91. doi:10.1097/00000441-200104000-00008. PMID 11307869. 
  4. ^ Roth BL (2007). "Drugs and valvular heart disease". N. Engl. J. Med. 356 (1): 6–9. doi:10.1056/NEJMp068265. PMID 17202450. 
  5. ^ Dahl CF, Allen MR, Urie PM, Hopkins PN (2008). "Valvular regurgitation and surgery associated with fenfluramine use: an analysis of 5743 individuals". BMC Med 6: 34. doi:10.1186/1741-7015-6-34. PMID 18990200. 

Further reading

  • Welch JT, Lim DS (November 2007). "The synthesis and biological activity of pentafluorosulfanyl analogs of fluoxetine, fenfluramine, and norfenfluramine". Bioorg. Med. Chem. 15 (21): 6659–66. doi:10.1016/j.bmc.2007.08.012. PMID 17765553. 

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